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. 2018 Jun 14;23(9):1851–1867. doi: 10.1038/s41380-018-0100-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Diazepam causes a time-dependent breakdown of GABAergic inhibitory synapses upon direct binding to GABA_ARs. a Immunolabeling of postsynaptic GABA_AR β_2/3-containing clusters (red) and VGAT-positive presynaptic GABAergic terminals (cyan) along MAP2-positive primary dendrites (20 µm; blue) of cortical neurons in the absence or presence of diazepam (D; 1 μM), and the corresponding graphs showing a decrease over time in b size (median/line-IQRs; mean/dot ± s.d. whiskers; Mann–Whitney test, *p < 0.05) and c number (mean ± s.e.m.; ANOVA/Bonferonni post-hoc test; *p < 0.05) of synaptic β_2/3 clusters, and d number of GABAergic terminals (mean ± s.e.m.; ANOVA/Bonferonni post-hoc test; *p < 0.05) contacting n = 59, n = 70, n = 53 control (DMSO)-treated primary dendrites and n = 70, n = 67, n = 44 diazepam-treated primary dendrites for 24 h, 48 h, and 72 h, respectively. Total of n = 17, n = 18 and n = 15 control and n = 17, n = 17 and n = 17 diazepam-treated neurons, respectively, collected from two independent experiments, were analysed in each group. e Representative traces of mIPSPs recorded in cortical neurons after 72 h treatment with control (DMSO) or diazepam (D; 1 μM), before and after application of isoguvacine ( + I, 50 μM), followed by picrotoxin ( + Pic, 50 μM; scale refers to all conditions), and corresponding bar graphs (mean ± s.d.; Student’s t-test: *p < 0.05) showing a diazepam-dependent decrease in f frequency and g amplitude of mIPSPs and the effects of isoguvacine ( + I, 50 μM; grey bars) from n = 7 control & n = 7 diazepam-treated cells collected from n = 3 independent experiments. h Immunolabelling of γ2-containing clusters (red) and VGAT-GABArgic terminals (cyan) along MAP2-positive dendrites (20 µm; blue) following 72 h treatment with control (DMSO), or diazepam (D; 1 μM), in the absence or presence of Ro 15-1788 (Ro; 25 μM), and the corresponding graphs showing a decrease in i size (median/line-IQRs; mean/dot ± s.d. whiskers; Mann–Whitney test, *p < 0.05), and j number of synaptic γ₂ clusters (mean ± s.e.m.; ANOVA/Bonferonni post-hoc test; *p < 0.05), and k decrease in the number of GABAergic terminals (mean ± s.e.m.; ANOVA/Bonferonni post-hoc test; *p < 0.05) contacting n = 49 control-treated & n = 45, n = 53, n = 48 diazepam-, diazepam/Ro- or Ro-treated dendrites for 72 h, respectively. The total of n = 15, n = 14, n = 13, n = 16 neurons, respectively, collected from two independent experiments, were analysed in each group. Scale bars = 20 μm (a, h-upper row) and = 5 μm (a, h-lower row)